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Article: Consumption of oxygen by astaxanthin biosynthesis: A protective mechanism against oxidative stress in Haematococcus pluvialis (Chlorophyceae)

TitleConsumption of oxygen by astaxanthin biosynthesis: A protective mechanism against oxidative stress in Haematococcus pluvialis (Chlorophyceae)
Authors
KeywordsAstaxanthin
Carotenogenesis
Haematococcus pluvialis
MRNA expression
Oxidative stress
Issue Date2008
Citation
Journal Of Plant Physiology, 2008, v. 165 n. 17, p. 1783-1797 How to Cite?
AbstractHaematococcus pluvialis, a unicellular green microalga, experiences photooxidative stress when exposed to excess photon flux density (PFD) relative to the capacity of photosynthesis, and particularly under other adverse environmental conditions (e.g., nutrient depletion, salinity, and excess heavy metals). Under stress, Haematococcus cells synthesize and accumulate large amounts of the secondary carotenoid astaxanthin stored in cytosolic lipid bodies. In this study, the transcriptional expression of five astaxanthin biosynthesis genes and two plastid terminal oxidase (PTOX) genes either in high PFD or in the presence of excessive sodium acetate and/or iron was determined by real-time reverse transcription PCR, and astaxanthin accumulation was measured by HPLC. Photosynthetic oxygen evolution, lipid peroxidation, and cell mortality were also investigated under these stress conditions. Our results indicate that the astaxanthin biosynthesis pathway may consume as much as 9.94% of the molecular oxygen evolved from photosynthesis under stress via at least two distinct routes: (1) extensive oxygen-dependent processes leading to astaxanthin formation, and (2) conversion of molecular oxygen into water using electrons derived from carotenogenic desaturation steps to PTOX via the photosynthetic plastoquinone (PQ) pool. Reduction of reactive oxygen species (ROS) production by reducing subcellular molecular oxygen substrates through the astaxanthin biosynthesis pathway may represent a novel protective mechanism to cope with oxidative stress. Reoxidation of the PQ pool by PTOX may further reduce photosynthetic electron transport chain-induced ROS formation. © 2008 Elsevier GmbH. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179081
ISSN
2021 Impact Factor: 3.686
2020 SCImago Journal Rankings: 1.032
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Yen_US
dc.contributor.authorSommerfeld, Men_US
dc.contributor.authorChen, Fen_US
dc.contributor.authorHu, Qen_US
dc.date.accessioned2012-12-19T09:51:49Z-
dc.date.available2012-12-19T09:51:49Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Plant Physiology, 2008, v. 165 n. 17, p. 1783-1797en_US
dc.identifier.issn0176-1617en_US
dc.identifier.urihttp://hdl.handle.net/10722/179081-
dc.description.abstractHaematococcus pluvialis, a unicellular green microalga, experiences photooxidative stress when exposed to excess photon flux density (PFD) relative to the capacity of photosynthesis, and particularly under other adverse environmental conditions (e.g., nutrient depletion, salinity, and excess heavy metals). Under stress, Haematococcus cells synthesize and accumulate large amounts of the secondary carotenoid astaxanthin stored in cytosolic lipid bodies. In this study, the transcriptional expression of five astaxanthin biosynthesis genes and two plastid terminal oxidase (PTOX) genes either in high PFD or in the presence of excessive sodium acetate and/or iron was determined by real-time reverse transcription PCR, and astaxanthin accumulation was measured by HPLC. Photosynthetic oxygen evolution, lipid peroxidation, and cell mortality were also investigated under these stress conditions. Our results indicate that the astaxanthin biosynthesis pathway may consume as much as 9.94% of the molecular oxygen evolved from photosynthesis under stress via at least two distinct routes: (1) extensive oxygen-dependent processes leading to astaxanthin formation, and (2) conversion of molecular oxygen into water using electrons derived from carotenogenic desaturation steps to PTOX via the photosynthetic plastoquinone (PQ) pool. Reduction of reactive oxygen species (ROS) production by reducing subcellular molecular oxygen substrates through the astaxanthin biosynthesis pathway may represent a novel protective mechanism to cope with oxidative stress. Reoxidation of the PQ pool by PTOX may further reduce photosynthetic electron transport chain-induced ROS formation. © 2008 Elsevier GmbH. All rights reserved.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Plant Physiologyen_US
dc.subjectAstaxanthin-
dc.subjectCarotenogenesis-
dc.subjectHaematococcus pluvialis-
dc.subjectMRNA expression-
dc.subjectOxidative stress-
dc.subject.meshCarotenoids - Biosynthesisen_US
dc.subject.meshCell Death - Drug Effectsen_US
dc.subject.meshChlorophyta - Cytology - Genetics - Growth & Development - Metabolismen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshGene Expression Regulation, Plant - Drug Effectsen_US
dc.subject.meshGenes, Planten_US
dc.subject.meshIron - Pharmacologyen_US
dc.subject.meshLipid Peroxidation - Drug Effectsen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshOxidative Stress - Drug Effectsen_US
dc.subject.meshOxygen - Metabolismen_US
dc.subject.meshOxygen Consumption - Drug Effectsen_US
dc.subject.meshPhotonsen_US
dc.subject.meshPhotosynthesis - Drug Effectsen_US
dc.subject.meshPlant Proteins - Metabolismen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshSodium Chloride - Pharmacologyen_US
dc.subject.meshStress, Physiological - Drug Effectsen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTranscription, Genetic - Drug Effectsen_US
dc.subject.meshXanthophylls - Biosynthesisen_US
dc.titleConsumption of oxygen by astaxanthin biosynthesis: A protective mechanism against oxidative stress in Haematococcus pluvialis (Chlorophyceae)en_US
dc.typeArticleen_US
dc.identifier.emailChen, F: sfchen@hku.hken_US
dc.identifier.authorityChen, F=rp00672en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.jplph.2007.12.007en_US
dc.identifier.pmid18313796-
dc.identifier.scopuseid_2-s2.0-51349091665en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-51349091665&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume165en_US
dc.identifier.issue17en_US
dc.identifier.spage1783en_US
dc.identifier.epage1797en_US
dc.identifier.isiWOS:000261059400003-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridLi, Y=8875807300en_US
dc.identifier.scopusauthoridSommerfeld, M=7007025132en_US
dc.identifier.scopusauthoridChen, F=7404907980en_US
dc.identifier.scopusauthoridHu, Q=26666082400en_US
dc.identifier.issnl0176-1617-

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